Graduate Studies Faculty

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J. Timothy Stout, MD, PhD, MBA

Vice President, Technology Transfer and Business Development
Professor, School of Medicine
Left OHSU per MMG
Admin Unit: SOM-Ophthalmology Department
Phone: 503-494-2435
Lab Phone: 503-494-6891
Fax: 503-494-7233
Office: Baird Hall 1027
Mail Code: L111
Programs:
Molecular & Medical Genetics
Program in Molecular & Cellular Biosciences
Research Interests:
ocular gene therapy age-related macular degeneration pediatric retinal disease inherited retinal disease
Preceptor Rotations
Dr. Stout has not indicated availability for preceptor rotations at this time.
Faculty Mentorship
Dr. Stout has not indicated availability as a mentor at this time.
Profile

One of the most common causes of human blindness is pathologic intraocular cellular proliferation. The abnormal proliferation of new blood vessels within the eye (ocular neovascularization) is the most common cause of permanent blindness in developed countries. Three diseases are associated with the vast majority of all cases of intraocular neovascularization: diabetes, retinopathy of prematurity and age related macular degeneration. While these three clinical entities are distinct and affect different groups of patients, they share a final common pathway which involves the uncontrolled division of endothelial cells leading to the formation of new blood vessels which ultimately compromise retinal function. Together, these conditions account for approximately 60% of untreatable blindness in the United States.
A major focus of our laboratory is to determine whether a variety of genes can be useful in modifying abnormal intraocular proliferation and, hence, decrease the stimulus towards neovascularization and blindness.
Our underlying hypothesis is that proteins, known to suppress unchecked endothelial cell division or aggregation, can be used to transform cells in vivo and arrest the development of retinal pathology. We employ viral and nonviral vectors to study the therapeutic efficacy of gene transfer in vivo. We have demonstrated an inhibitory effect on neovascularization in a variety of animal models germane to human disease.